Exam 3: Endocrine Disorders Flashcards
Adrenal Gland
Upper portion of the kidney
Consists of medulla and cortex
The Adrenal Medulla is essential for
essential for response to stress
The Medulla secretes
secrete catecholamines, neurotransmitters (epinephrine, NE and dopamine)
Adrenal Cortex
outer part, secretes adrenal hormones called corticosteroids
What corticosteroids does the adrenal cortex secrete?
A. Glucocorticoid (cortisol)
B. Mineralocorticoids (aldosterone)
C. Androgen
Addison’s Disease
HYPOFUNCTION OF ADRENAL CORTEX
- adrenocortical insufficiency, all three classes of adrenal corticosteroids are reduced
- autoimmune response
Causes of Addison’s Disease include
- Autoimmune (your own antibodies destroy your own adrenal cortex leading to a decrease in hormone production)
- Fungal infections
- AIDS
- Cancer
- Iatrogenic (anticoagulant, antineoplasm)
- Adrenalectomy
Clinical Manifestations of Addison’s Disease does not become evident until
until 90% of the adrenal cortex is destroyed
Primary clinical manifestations of Addison’s Disease include
- progressive weakness
- fatigue
- wt. loss
- anorexia
Other clinical manifestations of Addison’s Disease include
- skin hyperpigmentation (sun exposed areas) joint, pressure points palmar crease.
- Hypotension
- Hyponatremia (d/t opposite effect of mineralcorticoids)
- Hyperkalemia
- Nausea, vomiting, diarrhea (caused by hyperkalemia - increases peristaltic movement in GI)
Complications of Addison’s Disease include
Addisonian Crisis
Addisonian Crisis
Acute adrenal insufficiency triggered by stress or sudden withdrawal fo corticosteroid therapy
Symptoms of Addisonian Crisis include
- Hypotension (postural but from low fluid volume)
- Tachycardia (lack of aldosterone)
- Dehydration (d/t diarrhea from hyperkalemia)
- Hyponatremia (lack of aldosterone)
- Hyperkalemia
- Hypoglycemia (no production of glucocorticoids)
- Fever
- Weakness
- Confusion (d/t hypoglycemia - brain needs glucose)
Collaborative Care for Addison’s Disease includes
- daily glucocorticoid replacement (2/3 on awakening in AM 1/3 in late PM)
- shock management
- fluid replacement (large volume of 0.9% saline solution)
- mineralcorticoids – once daily in AM
Acute Intervention of patients with Addison’s Disease
- vital signs, fluid volume deficit / electrolytes, assess every 30 min to 4 hours for 1st 24 hours
- daily wt.
- corticosteroid administration
- keep follow up appointment
A patient with Addison’s disease should be protected against
protect against exposure to infection, noise, light and extreme temperature (could lead to addisonian crisis)
Ambulatory Care for Patients with Addison’s Disease
- carry a medic alert
- fluid replacement
- carry emergency kit (100mg IM hydrocortisone , syringe**)
Patient Teaching for Patient’s with Addison’s Disease
- Teach the importance of life long replacement therapy
- Teach additional exogenous corticosteroid adjustment secondary to stress
a. double dose when minor stress occurs
b. triple dose for major stress
Pheocromocytoma
- rare condition characterized by tumor of the adrenal medulla that produce excessive catecholamines (epinephrine, norepinephrine)
- results in severe hypertension
Clinical Manifestatons of Pheocromocytoma
- severe episodes of hypertension
* severe pounding headache*
* palpitation
* profuse sweating* - anxiety
- tachycardia*
Nursing Therapeutics/Collaborative Management for Pheocromocytoma
- surgical removal of tumor
- pre op sympathetic blocking agent (eg. Minipress, cardura) to decrease symptoms of catecholamine excess monitor for orthostatic hypotension
- metyrosine – adm. to diminish catecholamine production if surgery is not an option, may cause orthostatic hypotension
- monitor triad symptoms
- emotional support
Disorders Associated with ADH Secretions
- SIADH
- Diabetes Insipidus
ADH
Produced in hypothalamus and transported/stored in posterior pituitary gland.
Causes body to retain water and as a result there will be a decrease in urine output.
SIADH
Syndrome of inappropriate ADH.
Overproduction of ADH
Diabetes Insipidus
Underproduction or undersecretion of ADH
SIADH occurs when
ADH is release despite normal or low plasma osmolarity
SIADH is characterized by
- Fluid Retention
- Serum Hypoosmolarity
- Dilutional Hyponatremia
- Hypocholermia
- Concentrated urine in the presence of normal or increased intravascular volume and normal renal function
Causes of SIADH include
- malignant tumor (can produce and store, and release ADH)
- CNS Disorder (CVA, Head Injury)
- Drug Therapy (tegretol, diabenese, opoids, thiazides, tricyclic antidepressant
Clinical Manifestations of SIADH
• Extra cellular volume expands
• Plama osmoality declines
• Glomerular filtration rate increase (d/t high volume of fluid)
• Dilutional hyponatremia
• Low urine output, increase body wt.
• Vomiting, abdominal cramps, muscle twitching, seizure (d/t low sodium levels)
• Cerebral edema, lethargy, anorexia, confusion (d/t low sodium levels and water retention)
• Headache, seizure and coma (d/t cerebral edema)
NO PERIPHERAL EDEMA
Collaborative Care Goal for SIADH
Restore normal fluid volume osmolarity
Collaborative Care for SIADH include
- Restrict fluid intake to 800-1000 ml/day
- IV hypertonic solution , administer very slowly via pump
- Lasix to promote diuresis
Nursing Therapeutics for SIADH
- Assess v/s, I&O, daily wt.,LOC, s/s of hyponatremia, cardiac assessment
- Restrict fluid intake no more than 1000ml/day include meds
- Position of bed flat or no more than 10 degree elevation
- Seizure precaution
- Supplement diet with sodium
What should the nurse teach a patient with SIADH to do to decrease thirst?
Suck on hard candy to decrease thirst
Diabetes Insipidus
- Is a group of conditions associated with a deficiency of production or secretion of ADH or decrease renal response to ADH.
- lead to increase renal output and increase plasma osmolality
What are clinical manifestations of diabetes insipidus?
• polydipsia • polyuria (5-20 L/day) • very low specific gravity • elevated osmolality (due to pure water loss) SYMPTOMS D/T SEVERE DEHYDRATION: • nocturia, weakness (d/t large urine output during night time hours, weakness d/t dehydration and poor oxygen perfusion d/t Hypovolemia) • wt.loss, constipation • poor skin turgor • hypotension • tachycardia • shock
Collaborative Care Goal for Patients with Diabetes Insipidus
Maintain fluid and electrolyte balance
Collaborative Care for Diabetes Insipidus
- Hormonal Replacement
- Hypotonic Saline Administration IV or D5W (monitor glucose levels because hyperglycemia and glycosuria can lead to osmotic diuresis and increase fluid volume deficit)
- Drugs
- Sodium intake no more than 3 g/day
What drugs are used to treat diabetes insipidus?
Pitressin Diapid Indocin Tegretol Diabenese
Nursing Therapeutics for Patients with Diabetes Insipidus
- adequate p.o and IV hydration
- monitor urine for glucose if IVF glucose due to osmotic diuretic
- I & O, wt monitoring
Glucocorticoids
Regulates metabolism
Increases blood glucose levels
Critical in physiologic stress response.
Mineralcorticoids
Regulates Na and K balance
Androgens
Contribute to the growth and development of both genders and sexual activity in adult women.
Cushing’s Syndrome
Clinical abnormalities caused by EXCESS CORTICOSTEROIDS -> particularly glucocorticoids
What can cause Cushing’s?
- Iatrogenic administration of exogenous corticosteroids (prednisone)
- ACTH-secreting pituitary adenoma: stimulates glucocorticoids -> increase blood sugar
- Adrenal tumors and ectopic ACTH production by tumors outside of the hypothalamic-pituitary adrenal axis -> excess release of glucocorticoids
Clinical Manifestations of Cushing’s Disease
- Weight gain; BUFFALO HUMP in neck (d/t accumulation of adipose tissue in the trunk, face and cervical spine area)
- HYPERGLYCEMIA (d/t glucose intolerance and increased gluconeogenesis by the liver)
- Muscle wasting (weakness of extremities)
- Osteoporosis/pathological fracture (d/t loss of protein matrix in bone)
- Weak/thin Skin (d/t loss of collagen)
- MOON FACE (d/t increase in mineralcorticoids -> sodium and water retention)
- Mood disturbances
- Delayed wound healing
- Thinning hair
- Hypertension (sodium and water retention)
- Severe Acne
- Menstrual disorders, hirsutism in women
- Feminization, gynecomastia and impotence in men
The clinical presentation is the first indication of Cushing syndrome with particular importance on
(1) centripetal (truncal) obesity or generalized obesity;
(2) “moon facies” (fullness of the face) with facial plethora;
(3) purplish red striae (usually depressed below the skin surface) on the abdomen, breast, or buttocks;
(4) hirsutism in women;
(5) menstrual disorders in women;
(6) hypertension;
(7) unexplained hypokalemia
What can indicate Cushing;s Syndrome?
- 24 hour urine collection: >80-120 mcg
- Dexamethason Suppression Test
- MRI & CT of adrenal and pituitary gland
- Increased plasma ACTH = Cushing’s disease
- Decreased or normal ACTH = Cushing’s syndrome
Collaborative Care for Cushing’s Disease
- Primary goal is to normalize hormone secretion.
- Surgical removal of tumor (adrenalectomy)
- Drug therapy prior to surgery
Drug therapy prior to surgery for Cushing’s include
Mitotane and Ketoconazole
Mitotane
The inhibition of adrenal Function -> suppresses cortisol production and decrease plasma and urine corticosteroid levels.
Needed before surgery because surgery is a stressful event that increases cortisol production.
Ketoconazole
Blocks key enzymes in the body for essential production of corticosteroids.
Nursing Therapeutics for Cushing’s
- Monitor for S&S of thromboembolic events
- Emotional support -> body image disturbances
- Control of HTN, hyperglycemia and hypokalemia
Ambulatory home care for Cushing’s
- Stress may produce or precipitate acute adrenal insufficiency.
- Lifetime replacement therapy
- Wear medical alert bracelet
- Avoid exposure to extremes of temperature, infections and emotional disturbances
If pheocromocytoma is left untreated,
-Hypertensive Encephalopathy
-DM
-Cardiomyopathy
-Death
Can occur.
